Eosinophilia of the mucosa i.e. inflammation and thickening of airway,

Increased mucus secretion and

Contraction of smooth muscle of airways.

Hyperresponsiveness or hyperreactivity is the characteristic feature in asthma. This refers to the ease with which airways narrow in response to various nonallergic and nonsensitizing stimuli, including inhaled chemical mediators (e.g., histamine, methacholine) and natural physical stimuli (e.g. exercise, hyperventilation of cold air). It is likely that airway insult from chronic hyperresponsiveness early in life may lead to chronic changes in both lung structure and function.

Airway inflammation is a major contributor to the pathology of asthma. The inflammatory process includes infiltration of airways by eosinophils, activation of T cells and production of cytokines as well as other mediators involved in inflammation, an increase in mast cell numbers, and desquamation of airway epithelium. Chronic inflammatory process causes remodeling of the airways with mucosal thickening and smooth muscle hypertrophy even in mild asthmatics. Inflammation causes an associated increase in the existing airway hyperresponsiveness to a variety of stimuli.

Airway obstruction is due to narrowing of bronchioles and causes increased airway resistance, resulting in low forced expiratory volumes and flow rates. Obstruction causes premature closure of airways and air trapping. The blockage of airways from secretions and wall thickening causes atelectasis which leads V/ Q mismatch and the various changes in blood gases. Air trapping leads to hyperinflation and raised intrathoracic pressure, which in turn causes increase in work of breathing and may cause airleaks (pneumothorax, pneumomediastinum, subcutaneous emphysema). Increased intrathoracic pressure may cause hypotension by reducing venous return. Hypotension can cause hypoxia and decreased tissue perfusion and also affect the compliance.